This title appears in the Scientific Report :
2010
Please use the identifier:
http://dx.doi.org/10.1017/S0033291709992376 in citations.
Human amygdale reactivity is diminished by the beta-noradrenergic antagonist propranolol
Human amygdale reactivity is diminished by the beta-noradrenergic antagonist propranolol
Animal models of anxiety disorders emphasize the crucial role of locus ceruleus-noradrenergic (norepinephrine, NE) signaling, the basolateral amygdala (BLA) and their interactions in the expression of anxiety-like behavioral responses to stress. Despite clinical evidence for the efficacy of a β-nora...
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Personal Name(s): | Hurlemann, R. |
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Walter, H. / Rehme, A.K. / Kukolja, J. / Santoro, S.C. / Schmidt, C. / Schnell, K. / Musshoff, F. / Keysers, C. / Maier, W. / Kendrick, K.M. / Onur, O.A. | |
Contributing Institute: |
Kognitive Neurowissenschaften; INM-3 |
Published in: | Psychological medicine, 40 (2010) S. 1839 - 1848 |
Imprint: |
Cambridge
Cambridge Univ. Press
2010
|
Physical Description: |
1839 - 1848 |
PubMed ID: |
20102667 |
DOI: |
10.1017/S0033291709992376 |
Document Type: |
Journal Article |
Research Program: |
(Dys-)function and Plasticity Funktion und Dysfunktion des Nervensystems |
Series Title: |
Psychological Medicine
40 |
Subject (ZB): | |
Publikationsportal JuSER |
Animal models of anxiety disorders emphasize the crucial role of locus ceruleus-noradrenergic (norepinephrine, NE) signaling, the basolateral amygdala (BLA) and their interactions in the expression of anxiety-like behavioral responses to stress. Despite clinical evidence for the efficacy of a β-noradrenergic receptor blockade with propranolol in the alleviation of anxiety symptoms and the secondary prevention of post traumatic stress disorder, preclinical evidence for a β-noradrenergic modulation of BLA activity in humans is missing.We combined functional magnetic resonance imaging in healthy volunteers with probabilistic mapping of intra-amygdalar responses to fearful, neutral and happy facial expressions to test the hypothesis that a β-noradrenergic receptor blockade with propranolol would inactivate the BLA.Consistent with our a priori hypothesis, propranolol diminished BLA responses to facial expressions, independent of their emotional valence. The absence of activity changes in probabilistically defined visual control regions underscores the specific action of propranolol in the BLA.Our findings provide the missing link between the anxiolytic potential of propranolol and the biological basis of β-noradrenergic activation in the human BLA as a key target for the pharmacological inhibition of anxiety neurocircuitry. Moreover, our findings add to emerging evidence that NE modulates both the reactivity (sensitivity) and the operating characteristics (specificity) of the BLA via β-noradrenergic receptors. |